Abstract

AbstractThis study tests the hypothesis that perinatal taurine depletion impairs renal excretory function by increasing renin-angiotensin system (RAS) activity in adult female rats. Female Sprague-Dawley rats were fed normal rat chow and given water alone (C) or water containing 3 % beta-alanine (taurine depletion, TD) from conception until weaning. After weaning, the rats received normal rat chow and tap water with (CG, TDG) or without (CW, TDW) 5 % glucose. At 7–8 weeks of age, renal function at rest and after acute saline load was tested in conscious, restrained female rats with or without an angiotensin converting enzyme inhibitor captopril. Body, heart, and kidney weights were not significantly different among the eight groups. Compared to control, TD did not affect mean arterial pressure (MAP) or heart rate. Although captopril treatment significantly decreased MAP in all groups, the reduction was greatest in TDW. Further, the captopril treatment did not significantly affect renal blood flow, renal vascular resistance, glomerular filtration rate, filtration fraction, sodium and water excretion in TD compared to C groups, but did significantly decrease resting potassium excretion in CG. Fractional sodium and water excretion were markedly and significantly depressed after a saline load in CG, TDW, and TDG compared to CW groups. Captopril treatment depressed these responses in CW but not in CG, TDW, and TDG groups. Compared to the control, potassium excretion was not altered by captopril treatment. These data indicate that in adult female rats, perinatal taurine depletion depresses the renal excretory effect of RAS, independent of high sugar intake.KeywordsAdultFemaleKidneyPerinatal taurineRatRenin-angiotensin system

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